Changing the Tendency to Integrate the Senses.

Integration of sensory signals that emanate from the same source, such as the visual of lip articulations and the sound of the voice of a speaking individual, can improve perception of the source signal (e.g., speech). Because momentary sensory inputs are typically corrupted with internal and external noise, there is almost always a discrepancy between the inputs, facing the perceptual system with the problem of determining whether the two signals were caused by the same source or different sources. Thus, whether or not multisensory stimuli are integrated and the degree to which they are bound is influenced by factors such as the prior expectation of a common source. We refer to this factor as the tendency to bind stimuli, or for short, binding tendency. In theory, the tendency to bind sensory stimuli can be learned by experience through the acquisition of the probabilities of the co-occurrence of the stimuli. It can also be influenced by cognitive knowledge of the environment. The binding tendency varies across individuals and can also vary within an individual over time. Here, we review the studies that have investigated the plasticity of binding tendency. We discuss the protocols that have been reported to produce changes in binding tendency, the candidate learning mechanisms involved in this process, the possible neural correlates of binding tendency, and outstanding questions pertaining to binding tendency and its plasticity. We conclude by proposing directions for future research and argue that understanding mechanisms and recipes for increasing binding tendency can have important clinical and translational applications for populations or individuals with a deficiency in multisensory integration.

Mechanical injury and blood are drivers of spatial memory deficits after rapid intraventricular hemorrhage.

Aneurysmal intraventricular hemorrhage (IVH) survivors may recover with significant deficits in learning and memory. The goal of this study was to investigate the mechanism of memory decline after intraventricular aneurysm rupture. We developed an aneurysmal IVH rat model by injecting autologous, arterial blood over the period of two minutes into the right lateral ventricle. We also evaluated the effects of a volume-matched artificial cerebrospinal fluid (CSF) control, thrombin and the mode of delivery (pulsed hand injection versus continuous pump infusion). We performed magnetic resonance brain imaging after 1 and 5 weeks to evaluate for hydrocephalus and histological analysis of the dentate gyrus after 6 weeks. Only animals which underwent a whole blood pulsed hand injection had a spatial memory acquisition and retention deficit 5 weeks later. These animals had larger ventricles at 1 and 5 weeks than animals which underwent a continuous pump infusion of whole blood. We did not find a decline in dentate gyrus granule cell neurons or an impairment in dentate gyrus neurogenesis or differentiation 6 weeks after IVH. Rapid injections of blood or volume resulted in microglial activation in the dentate gyrus. In conclusion, our results point to mechanical injury as the predominant mechanism of memory decline after intraventricular aneurysmal rupture. However, volume-matched pulsed injections of artificial CSF did not create a spatial memory deficit at 5 weeks. Therefore, whole blood itself must play a role in the mechanism. Further research is required to evaluate whether the viscosity of blood causes additional mechanical disruption and hydrocephalus through a primary injury mechanism or whether the toxicity of blood causes a secondary injury mechanism that leads to the observed spatial memory deficit after 5 weeks.

Bioengineering an Artificial Human Blood⁻Brain Barrier in Rodents.

Our group has recently created a novel in-vivo human brain organoid vascularized with human iPSC-derived endothelial cells. In this review article, we discuss the challenges of creating a perfused human brain organoid model in an immunosuppressed rodent host and discuss potential applications for neurosurgical disease modeling.